During the past decade, a substantial amount of knowledge concerning the complex interaction between cardiac muscle and left ventricular growth has been accumulated. Although it is now generally held that many types of cardiac hypertrophy significantly and adversely alter the coronary circulation and the electrophysiological characteristics of hypertrophied cardiac muscle, many important areas remain to be explored. This proposal has four major goals: 1) to define the segment or segments in the coronary arterial microvasculature responsible for the increased minimal coronary vascular resistance observed when left ventricular hypertrophy occurs in response to systemic hypertension. These studies will employ a unique technology for measuring microvascular pressure and diameter in arterials down to 100 microns in size in the beating left ventricle; 2) to determine if left ventricular hypertrophy secondary to renal hypertension impairs the development of mature coronary collateral vessels. Because coronary growth is limited in hypertrophied ventricles, we postulate that coronary collateral growth may also be impaired; 3) to assess the effects of autonomic tone and increases in left ventricular pressure on the electrophysiological characteristics of ischemic cardiac muscle in normal and hypertrophied hearts; and 4) to study the pathophysiology of reactive hypertrophy that develops in patients with acute myocardial infarction. In these studies, changes in left ventricular mass will be measured over time with a unique and precise method of defining left ventricular mass (cine computed tomography). Also, coronary reserve in angiographically normal vessels perfusing hypertrophied muscle in patients with previous myocardial infarction will be studied utilizing an intracoronary Doppler catheter and maximal coronary dilation with intracoronary papaverine. In the aggregate, these four groups of studies will further our understanding about the complex effects of cardiac hypertrophy on the coronary circulation and the electrical stability of the myocardium.